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Biomedical subjects

M P Iavich

Publications and source records attributed to M P Iavich.

At least 19 recordsLinked to original sources
PubMed1988

[Elimination of stress-induced activation of DNA reparative synthesis in the myocardium by increasing the load on the heart].

The rate of DNA reparative synthesis was studied in the nucleus of myocardial cells in the heart compensatory hyperfunction (HCH) induced by the aorta coarctation and in animals exposed to surgical stress without the aorta coarctation. It was established that both surgery and emotional painful stress activated the DNA reparative synthesis in myocardial cells. For example, 12-24 hrs following the surgery the DNA reparation rate exceeded control values by 50-74%. HCH induced no changes in the DNA reparation rate in nuclei of myocardial cells. The mechanism of stress-induced DNA damage is discussed and a hypothesis is put forward on stabilizing the effect of hyperfunction on the DNA structure.

Animals↗
PubMed1983

[Molecular mechanisms of myocardial hypertrophy and deterioration].

The development of cardiac compensatory hypertrophy (CCH) during heart adaptation to increased load is conditioned by two simultaneous processes which are accelerated synthesis and slower degradation of protein. In CCH, increased protein-synthesizing capacity of the myocardium is based on accelerated transcription. At the same time, the rates of rRNA and mRNA degradation are increased at the emergency stage of CCH. Organ-nonspecific cytoplasmic protein factors are identified that take part in the mechanism which initiates accelerated transcription during CCH. Along with total transcription acceleration, a selective activation of structural genes which code the most effective isoenzymes occurs in the heart at the emergency stage. A standard complex of biochemical changes in myocardial metabolism is shown to occur at the stage of wear and during physiological ageing: RNA concentration is decreased, the rates of its synthesis and degradation are reduced, as are the rates of protein synthesis and degradation. At the same time, administration of tRNA to animals accelerates protein synthesis in such a heart.

Aging↗
PubMed1981

[Ratio of the amounts of the mRNA poly A+/poly A- fractions in the myocardium and the life span of mRNA poly A+].

Two mRNA fractions, poly A+ and poly A- were found in the rat heart muscle. They comprise 30 and 70% of the entire mRNA, respectively. The ratio of the mRNA poly A+ to poly A- in the myocardium does not change in physiological aging. According to the kinetics of labelled precursor incorporation into mRNA, the life span of the main mass of mRNA poly A+ in the myocardium is about 4 hours.

Aging↗
PubMed1976

[Influence of aging on synthesis and breakdown of RNA and protein in the myocardium].

The rate of decomposition of RNA and proteins in the heart muscle of aged rats, as well as the effect of t-RNA on the rate of translation in the reconstructed non-cellular system of protein synthesis were studied. The rate of decomposition of sarcoplasmatic and myofibrill proteins and RNA is known to be decreased in the heart muscle of old animals. The metabolic changes. The addition of homologous t-RNA to the non-cellular system of protein synthesis was shown to stimulate the incorporation of labelled amino acids into the ribosomes of the heart of old rats.

Aging↗
PubMed1976

[In vitro incorporation of labelled amino acids into heart muscle ribosomes at early and late stages of compensatory heart hyperfunction].

The activity of a protein-synthesizing cell-free system from heart muscle was studied at early and late stages of compensatory heart hyperfunction. It was found that the incorporation of amino acids into heart ribosomes during 48 hours after the hyperfunction had been produced, increased by 30% as compared to the control. The incorporation of amino acids into heart ribosomes at the late stage of hyperfunction (after 6 months) was decreased by 46% as compared to the early stages. The addition of homologous tRNA to the cell-free system of protein synthesis under prolonged heart hyperfunction stimulated the incorporation of amino acids into the ribosomes by 40--50%.

Amino Acids↗
PubMedDate not supplied

[Cell-free system of protein synthesis from rat's cardiac muscle].

A cell-free system of protein synthesis from rat heart muscle is described. The system contained preparations of ribosomes, which were not separated from myofibrillar proteins. The conditions for incorporation of 14C-leucine into the polyribosomes of the fraction were established and its protein synthetizing activity was studied.

Animals↗
PubMedDate not supplied

[Metabolic stability of the protein-synthesizing system of the myocardium in compensatory cardiac hyperfunction in actinomycin D block of RNA synthesis].

Under conditions of complete actinomycin block in rat heart muscle an inhibition of protein synthesis and dissociation of myocardial polyribosome structures were observed (half-life was equal to 6.5 hrs). In compensatory hyperfunction of heart muscle, caused by stenosis of aorta, the inhibitory effect of actinomycin D on the protein synthesis was manifested earlier than in control and was exhibited more distinctly. In myocardium under compensatory hyperfunction of heart muscle the protein synthesis was decreased by 50% within 4 hrs after administration of actinomycin into animals and it was completely inhibited within 10 hrs after the antibiotic administration. The alteration in stability of polyritobosomes under compensatory hyperfunction of heart muscle was specific for myocardium and was not observed in liver tissue.

Adaptation, Physiological↗
PubMedDate not supplied

[RNA and protein metabolism in the myocardium in aging and long-term hyperfunction of the heart].

Metabolism RNA and proteins was distinctly altered in myocardium hypertrophied due to prolonged hyperfunction and in the heart muscle of aged rats. The following alterations were observed: decrease in RNA concentration and in the absolute rate of protein synthesis in vivo, decrease in incorporation of labelled amino acids into heart ribosomes in cell-free system, the distinct depression of RNA turnover. The data obtained suggest that prolonged heart hyperfunction and hypertrophy promote the myocardium impairment and hence the process of senescence in developed more rapidly than under normal conditions.

Aging↗
PubMedDate not supplied

[Metabolism of myocardial poly A+-containing mRNA normally and in compensatory cardiac hyperfunction].

Two fractions of mRNA--polyA+ and polyA- containing mRNA--were found in rat heart muscle by affinity chromatography using polyU cellulose. These fractions constituted 30% and 70% of total mRNA, respectively. The ratio of polyA+/polyA- mRNA was not altered in myocardium under heart hyperfunction and in physiological ageing. Duration of life of polyA+ containing mRNA was 4 hrs in normal heart. A; the beginning of myocardium hyperfunction the period of mRNA life was decreased down to 2-3 hrs; this pattern of mRNA life alteration did not differ from control one in prolonged heart hypertrophy within 6 months. The rate of polyA+ containing mRNA synthesis was increased by 70% at the early steps of heart hyperfunction as compared with normal state; it decreased below the normal state in long-term hypertrophy of myocardium. In development of heart hyperfunction acceleration of polyA+ containing mRNA synthesis was more distinct than an increase in rRNA synthesis.

Animals↗
PubMedDate not supplied

[The effect of surgical stress on DNA synthesis in liver and brain cells].

Distinct alterations in the rate of DNA synthesis (an increase in the rate of reparation and a decrease in the rate of replication in nuclei and mitochondria) were detected in liver and brain cells during the stress caused by surgical operation. Within 8-10 hrs after the operation the rate of DNA reparation was increased by 40-50% in nuclei of liver cells and by 31-35% in brain cell nuclei. Replication of nuclear DNA was decreased immediately after the operation--by 33% in liver cells and by 50% in brain cells. Within a day after the operation the rate of replication was restored up to the control level in liver cells, while it was still decreased by 30% in brain cells. The rate of mitochondrial DNA synthesis was slightly decreased within the first 12 hrs after the operation: by 12-14% in liver cells and by 18-20% in brain cells. The stress, and particularly postoperative stress, exhibited pronounced action on structure and various systems of DNA synthesis in cells of various tissues.

Animals↗
PubMedDate not supplied

[The role of cytoplasmatic factors in post-stress changes in the RNA synthesis in the heart and liver].

Effect of protein factors from heart and liver cytoplasm (S-100 fraction) on activity of RNA polymerases I and II was studied in isolated nuclei of heart and liver tissues under conditions of immobilization stress. Activity of the cytosol factors, stimulating ribosomal RNA (rRNA) synthesis, was altered during the post-stressory period. Immediately after immobilization the activity of the cytosol was decreased at the catabolic phase. Within a day the activity was distinctly increased at anabolic phase of the stressory reaction. The active post-stressory cytosol was studied in the cell-free system containing nuclei from heart and liver tissues of animals subjected to stress and of the control animals. The active post-stressory cytosol increased the rate of rRNA synthesis in corresponding nuclei of heart and liver tissue, while synthesis of rRNA was increased 2-fold in nuclei of control animals as compared with heart and liver nuclei, isolated within a day after termination of stress. Activation of the cytoplasmic factors stimulating the transcription rate is concluded to be of importance for regulation of rRNA synthesis under adaptation conditions.

Animals↗
PubMedDate not supplied

[DNA synthesis in heart cells in its compensatory hyperfunction].

In modelling compensatory hyperfunction of the heart (CHH) due to coarctation of the aorta, the replication rate in the nuclei of myocardial cells increases in 24 hours and becomes 20 fold the control values in 48 hours. The replication rate in myocardial mitochondria in CHH reduces at the beginning of hyperfunction but increases almost two fold in 48 hours. The DNA reparation rate in the nuclei of the myocardial cells does not change in CHH. The rate of this process, however, increases significantly (by 50-74%) in cardiac cells of animals subjected to operation but without coarctation of the aorta.

Animals↗
PubMedDate not supplied

[Suppression of replication and activation of DNA reparative synthesis in stress and prevention of these phenomena by preliminary adaptation].

Effects of preliminary adaptation to short-term stress or to regular hypoxia on disturbances of DNA biosynthesis were studied in liver and heart tissues under conditions of emotional-painful stress (EPS). EPS was found to induced activation of DNA reparative synthesis in heart and liver tissues and affected dissimilarly DNA replication in these tissues: activation of the reaction in heart and suppression in liver tissue. Adaptation to regular hypoxia limited distinctly the burst of DNA reparative synthesis in cells of both these tissues, reduced activation of the DNA replicative synthesis in heart and prevented the stress induced depression of DNA replication in hepatic cell nuclei and mitochondria. Mechanisms of the hepatoprotective effect of adaptation to hypoxia is discussed.

Adaptation, Physiological↗
PubMedDate not supplied

[The effect of emotional-pain stress on the rate of DNA synthesis in heart and liver cells].

Effect of a single long-term (6 hrs) emotional-painful stress on DNA synthesis was studied in nuclei and mitochondria of heart and liver cells. Various systems of DNA synthesis in heart and liver cells were shown to respond dissimilarly to the stress. The rates of replication and reparative synthesis of nuclear DNA were increased while synthesis of mitochondrial DNA was unaltered in heart cells within the first day after the stress. In liver cells the reparative synthesis of nuclear DNA was also increased, whereas the rate of its replication in nuclei and mitochondria was distinctly inhibited for a long time. Thus, the systems of DNA synthesis in liver cells proved to be more sensitive to extreme stress-reactions as compared with heart cells. Effect of the stress on the systems of DNA synthesis in specific and connective tissue cells of liver and heart is discussed. At the same time, mitochondria are localized in specialized cells of both heart and liver tissues. The data obtained suggest that inhibition of the mitochondrial DNA synthesis is realized in hepatocytes.

Animals↗